An animal model of acute hepatic failure which closely resembles human fulminant hepatic failure has been developed in an inbred strain of rabbits using the selective hepatotoxin galactosamine. An extracorporeal hepatic support system for the removal of potentially encephalopathic substances from the plasma of rabbits has been developed. If certain specific surfaces are incorporated into this device, hemoperfusion results in complement activation, the pulmonary sequestration of aggregated neutrophils and death. Large doses of hydrocortisone do not prevent this syndrome. The recording of repeated visual evoked potentials in the central nervous system is a reliable, quick, non-invasive method of quantifying neurologic changes in hepatic encephalopathy. Serum levels of gamma aminobutyric acid (GABA), a major inhibitory neurotransmitter, are increased in acute hepatic coma. The main source of GABA in peripheral blood is the enteric bacterial flora. The density of receptors for GABA on postsynaptic neural membranes is increased in acute hepatic coma.